Band 3 (SLC4A1) Rabbit Polyclonal Antibody

CAT#: TA381670

SLC4A1 Rabbit polyclonal Antibody

Specifications

Product Data

• Applications: IF, WB
• Recommended Dilution: WB,1:500 - 1:2000
  IF,1:50 - 1:200
• Reactivities: Human, Mouse, Rat
• Host: Rabbit
• Isotype: IgG
• Clonality: Polyclonal
• Immunogen: Recombinant fusion protein containing a sequence corresponding to amino acids 1-353 of human SLC4A1 (NP_000333.1).
• Formulation: Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3.
• Concentration: lot specific
• Purification: Affinity purification
• Conjugation: Unconjugated
• Stability: Shelf life: one year from despatch.
• Gene Name: solute carrier family 4 member 1 (Diego blood group)
• Database Link:
  Entrez Gene 6521 Human
  UniProt ID P02730
• Background: The protein encoded by this gene is part of the anion exchanger (AE) family and is expressed in the erythrocyte plasma membrane, where it functions as a chloride/bicarbonate exchanger involved in carbon dioxide transport from tissues to lungs. The protein comprises two domains that are structurally and functionally distinct. The N-terminal 40kDa domain is located in the cytoplasm and acts as an attachment site for the red cell skeleton by binding ankyrin. The glycosylated C-terminal membrane-associated domain contains 12-14 membrane spanning segments and carries out the stilbene disulphonate-sensitive exchange transport of anions. The cytoplasmic tail at the extreme C-terminus of the membrane domain binds carbonic anhydrase II. The encoded protein associates with the red cell membrane protein glycophorin A and this association promotes the correct folding and translocation of the exchanger. This protein is predominantly dimeric but forms tetramers in the presence of ankyrin. Many mutations in this gene are known in man, and these mutations can lead to two types of disease: destabilization of red cell membrane leading to hereditary spherocytosis, and defective kidney acid secretion leading to distal renal tubular acidosis. Other mutations that do not give rise to disease result in novel blood group antigens, which form the Diego blood group system.One null mutation in this gene is known, resulting in very severe anemia and nephrocalcinosis.